Toxicology Case: The poison in the pond: Blue-green algae toxicosis in a young dog - Veterinary Medicine
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Toxicology Case: The poison in the pond: Blue-green algae toxicosis in a young dog


VETERINARY MEDICINE


DISCUSSION

Blue-green algae are members of the phylum Cyanobacteria. Some species of cyanobacteria can produce toxins. They are microscopic organisms that form visible colonies in water under favorable conditions (stagnant water, fertilizer runoff) mostly during hot-weather months. The case discussed here occurred in July.

Blue-green algae blooms—large accumulations of algae—can occur in lakes, ponds, or rivers. These blooms are usually dark green or sometimes reddish brown. The wind propels the toxic algae to the shoreline where animals are exposed when they drink blue-green algae-contaminated water. Dogs are affected when they swim and drink contaminated water or when they eat toxin-producing algae.1

Toxicity

Common toxin-producing genera of cyanobacteria include Microcystis, Anabaena, Oscillatoria, Aphanizomenon, Nodularia, and Nostoc species. Four types of toxins are known to be produced by cyanobacteria, but the two main types are hepatotoxins and neurotoxins.

Hepatotoxin peptides (heptapeptides or pentapeptides) are the most common cause of blue-green algae poisoning in animals.1 Hepatotoxicosis from hepatotoxic peptides is characterized by signs of vomiting, diarrhea, anorexia, lethargy, hepatopathy, and acute hepatic failure as well as death.

The most common neurotoxins that cyanobacteria produce are alkaloids anatoxin-a and anatoxin-a(s). Anatoxin-a is the most common neurotoxin. It is a strong postsynaptic depolarizing neuromuscular blocking agent that affects nicotinic and muscarinic acetylcholine receptors. Anatoxin-a(s) inhibits peripheral cholinesterase irreversibly. Blue-green algae neurotoxins interfere with neurotransmission across neurons or neuromuscular junctions, causing central nervous system (CNS) signs and death due to respiratory failure.1-3

Neurotoxicosis due to blue-green algae is potentially lethal, although few cases of this poisoning in dogs have been reported in North America.2 The lethal oral dose in dogs is not known. In mice, the approximate oral LD50 of anatoxin-a is 5 mg/kg. In dogs, anatoxin-a ingestion is known to cause muscle fasciculations, seizures, collapse, weakness, respiratory failure, and death within 10 minutes to a few hours of exposure.2,3

The slight increase in alkaline phosphatase activity noted in this case may have been due to muscular activity or anoxia during seizures, whereas the slight increase in alanine transaminase activity could be due to phenobarbital administration.

Differential diagnoses

In cases similar to this one, possible differential diagnoses should include mushroom, metaldehyde, or strychnine poisoning; water intoxication; pesticide poisoning (organophosphates, carbamates or organochlorines, pyrethrins or pyrethroids); metabolic or infectious disease; and head trauma.

Diagnosis

A tentative diagnosis is based on a history of exposure (swimming in or drinking lake or pond water, algae on the fur or muzzle or in the vomitus) and the rapid onset of neurologic signs (vomiting, ataxia, seizures, respiratory failure) or death.1

Initial clinical signs of blue-green algae poisoning in dogs due to either hepatotoxicosis or neurotoxicosis may be similar. However, with hepatotoxicosis, within hours of exposure, there are signs of liver failure accompanied by many-fold increases in liver-specific enzyme activities such as alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and coagulopathy (increased prothrombin time, activated partial thromboplastin time). With neurotoxicosis, marked increases in liver enzyme activities are not seen during the course of illness.

Unfortunately, there are no widely available, rapid, inexpensive tests available to confirm blue-green algae toxicosis.4 To definitively diagnose blue-green algae poisoning—after providing treatment—submit pond water and stomach contents for microscopic identification of toxigenic algae. Specimens (1 to 2 L of algae obtained by straining through cheese cloth) can be sent to a veterinary diagnostic laboratory for identification, purification, and quantification of algal toxins or mouse bioassay or for enzyme-linked immunosorbent assay.1

In a recently published case report, anatoxin-a was detected in the urine and bile of a dog that had been euthanized because of neurotoxic blue-green algae exposure.2 In the case reported here, the presence of neurotoxic blue-green algae toxins was not confirmed.

Treatment

Suspected poisoning cases must be treated aggressively and quickly before a definitive diagnosis is established. The main goals of treatment are decontamination, seizure control, respiratory support, and supportive care.

Because of the rapid onset of clinical signs, inducing emesis may not be feasible or practical. However, in asymptomatic dogs, emesis can be induced with hydrogen peroxide (2.2 ml/kg orally, repeat once if emesis is unsuccessful the first time) or apomorphine (0.04 mg/kg intravenously, or dissolve part of a pill and instill subconjunctivally and rinse after emesis has occurred) followed by activated charcoal (2 to 4 g/kg).

Give diazepam (0.5 to 2 mg/kg intravenously), propofol (3 to 6 mg/kg intravenously or 0.1 to 0.6 mg/kg/min CRI), or phenobarbital (2 to 5 mg/kg intravenously) to control seizures. However, if the patient's respiratory system is compromised, avoid giving phenobarbital or propofol. Place a cuffed endotracheal tube and provide assisted respiration if needed, such as in this case.

Give atropine sulfate (0.04 to 0.1 mg/kg intravenously) to control muscarinic signs such as hypersalivation, bradycardia, and increased bronchial secretions. Antiemetics (maropitant 1 mg/kg subcutaneously once a day) and broad-spectrum antibiotics can be given as needed.

Monitoring

Perform a CBC and serum chemistry profile at presentation and every 24 hours for two or three days or as long as needed. Monitor blood glucose concentrations, hematocrit, and blood gases in symptomatic cases.

SUMMARY

After ingesting neurotoxic blue-green algae, dogs can develop life-threatening clinical signs quickly. Providing ventilator support to these dogs for extended periods may be critical for successful treatment outcomes.

Safdar A. Khan, DVM, MS, PhD, DABVT
ASPCA Animal Poison Control Center
1717 S. Philo Road, Suite 36
Urbana, IL 61802

To view the references for this article, visit http://dvm360.com/AlgaeToxRefs.


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Source: VETERINARY MEDICINE,
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